Prostaglandin E2 support of adrenal medullary release of epinephrine in anephric dogs.
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Biomedical subjects
Publications and source records attributed to T S Harrison.
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Although the unique sensitivity of blood pressure to hemorrhage after adrenalectomy can be overcome by adrenocortical hormones the specificity of this steroid effect is not known. Under pentobarbital anesthesia five groups of six adult male Sprague-Dawley rats were bled into a 0.9% saline-primed pressure-balanced reservoir. A mean arterial pressure of 50 Torr was maintained for 3 h. When compared to normal rats, those with adrenalectomy showed significantly lowered bleeding volume (P less than 0.05 to less than 0.001). In untreated adrenalectomized rats 120 min following hemorrhage, saline was consistently taken up from the reservoir to maintain blood pressure at 50 Torr. Deoxycorticosterone-cortisol (intravenous bolus coupled with infusion) restored bleeding volume to normal in adrenalectomized rats. Aldosterone (constant infusion) also protected bleeding volume after adrenalectomy, P less than 0.05 to less than 0.01, but this effect was significantly less striking than that of cortisol 180 min after the onset of bleeding, P less than 0.001. Sham adrenalectomy did not affect bleeding volume. Aldosterone appears to be effective in restoring normal bleeding volume sensitivity after adrenalectomy but this effect of aldosterone is less sustained than that seen with cortisol.
This study was performed to determine whether or not the adrenal medulla supports cardiac output and total peripheral vascular resistance after acute hypovolemia. Two groups of anesthetized dogs were studied. The first group underwent right adrenalectomy and the second, left adrenal denervation in addition. Adrenocortical function, as reflected by compound F and dihydroepiandrosterone determinations, was equally maintained in both groups for 120 minutes after hemorrhage. Arterial plasma concentrations of norepinephrine and epinephrine were low in group 2, p greater than 0.05 to greater 0.01. Cardiac index and peripheral vascular resistance were comparable in both groups before and for two hours after the induction of hypovolemia to a mean arterial pressure of 50 millimeters of mercury. The findings indicate that cardiac output and total peripheral resistance do not require adrenomedullary catecholamine release after acute hypovolemia.
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A severe rebound rise in blood pressure with agitation and insomnia had been noted in five patients when they had previously ceased clonidine (Catapres) This has been shown to be reproducible in these patients and to be associated with a significant increase in urinary catecholamine excretion. The blood pressure can be controlled and the symptoms alleviated promptly by alpha and beta adrenergic receptor blockade using intravenous phentolamine and propranolol.
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